The overall goal of this project is to advance our understanding of the auditory-signal-processing roles played by the interactions between the anteroventral and dorsal cochlear nucleus (AVCN and DCN). Existing information clearly indicates that anatomical connections do exist from the DCN to the AVCN and vice versa. The DCN-to-AVCN and AVCN-to-DCN interactions will be investigated physiologically in the present project, while the same structures will be investigated anatomically and immunocytochemically in another project headed by Dr. Morest. The experimental design and data analyses of these two projects will be closely coordinated with extensive collaboration. The first aim of the present project is to elucidate inhibitory and/or excitatory effects on responses of single primarylike and chopper units (putative bushy and stellate cells) in the AVCN exerted by inputs from the DCN. This study will evaluate the "neural gate" and "echo suppression" hypotheses in vivo by recording single unit responses in the AVCN of unanesthetized decerebrate cats to the same acoustic signals as used in human psychophysical "gating" or "echo suppression" paradigms. While recording from a single unit in the AVCN, a localized region of the DCN, where the characteristic frequency (CF) for multiunit cluster activities is equal to that of an AVCN unit under recording, will be excited or inhibited with microinjections of excitatory or inhibitory chemical agents, i.e., glutamate, glycine or gamma-aminobutyric acid (GABA). We will also use knife cuts of the DCN-to-AVCN connections. The second aim is to elucidate inhibitory and/or excitatory effects on responses of single units in the DCN, particularly type II units (putative corn cells), exerted by inputs from the AVCN. A distinct feature of a type II DCN unit's behavior is that, although it is excited by a narrow-band stimulus, such as a pure tone at the unit's CF, it is not excited at all by a wide-band noise at any level. It is hypothesized that this behavior of a type II unit arises from inhibitory inputs to a type II unit from neurons with a wide range of CFs. The proposed study will evaluate the hypothesis that the AVCN is a source of such inhibition by determining whether a type II DCN unit becomes excited by a wide-band noise when the AVCN-to-DCN inputs are blocked. The third aim is to relate the above physiological findings to the anatomical and immunocytochemical findings of Project 1 by conducting combined physiological and anatomical experiments. The new knowledge about the auditory system function to be gained from the present research should be valuable in the long run as a systematic guide in the development of improved diagnostic and prosthetic devices and methods for management of people with sensorineural hearing impairments.